Plasma osmolality (pOsmol) and neurohumoral signals play important roles in the pathophysiology of cardiovascular diseases. Our study investigated the effect of high environmental temperature (HET) on neurohumoral responses and pOsmol in rats fed a high salt diet (HSD), with and without angiotensin II receptor blockade (ARB), using telmisartan.  Fifty-six male 8-week old Sprague-Dawley rats (95-110g) were randomly assigned into seven groups of 8 rats. These included control rats (I) fed with 0.3% NaCl diet (normal diet, ND); salt-loaded rats (II) fed with 8% NaCl (high salt) diet; ND rats (III) exposed to HET (38.5±0.5oC ) 4 hours daily per week; rats (IV) fed with 8% NaCl diet and exposed to HET daily. Others included rats (V) fed with 8% NaCl diet and treated with telmisartan (30mg/kg); ND rats (VI) exposed to HET and treated with telmisartan; rats (VI) fed with 8% NaCl diet, exposed to HET and treated with telmisartan. Plasma angiotensin II, aldosterone, vasopressin and norepinephrine (NE) concentrations were determined by ELISA technique; pOsmol from plasma K+, Na+ and Urea. HSD combined with HET in rats synergistically increased pOsmol (P<0.001) with an associated non-synergistic rise in fluid intake (P<0.001), fluid balance (P<0.001), plasma angiotensin II (P<0.01) and aldosterone (P<0.05), NE (P<0.001) and vasopressin (P<0.05) concentrations compared to control. Telmisartan did not alter pOsmol in all the treated-rats, but normalized fluid intake levels and plasma vasopressin in the rats exposed to either HSD or HEt alone. Prolonged exposure of rats to hot environment exacerbated the effect of excess dietary salt on pOsmol, with no effect on angiotensin II-mediated neurohumoral responses

Oxidative stress, heat shock protein (HSP70) and p38 mitogen-activated protein kinase (MAPK) are important functional cellular signals involved in the pathophysiology of cardiovascular diseases. This study investigated the effect of high environmental temperature (HET) and high salt diet (HSD) respectively and together on systemic oxidative stress, nitric oxide (NO), HSP70 and renal p38 MAPK. Methods: Thirty-two male Sprague-Dawley rats were divided into four groups with eight rats in each group: Control rats (C) fed a normal diet; salt-loaded rats (S) fed a HSD (8%NaCl); normal diet rats (H) exposed to HET (38.5 ± 0.5 o C 4h daily for 8weeks); and salt-loaded rats (SH), fed a HSD and exposed to HET. Circulatory oxidative stress parameters (SOD: superoxide dismutase; GSH: glutathione; CAT: catalase; MDA: malondialdehyde), HSP70 and renal p38 MAPK were determined by colorimetric, enzyme-linked immunosorbent assay (ELISA) methods and immunohistochemistry (IHC) techniques respectively. Results: Plasma GSH concentration and CAT activity decreased significantly, with significant increase in MDA concentration in all the rat groups compared to control. However, MDA in SH rats was significantly higher than in either S or H rats. Circulatory HSP70 and NO were significantly raised in S and H rats but unchanged in SH rats compared to control. Conversely, renal expression of p38 MAPK was significantly increased in H and SH rats compared to control, but SH rats had significantly higher level than either S or H rats. SH rats also had weight gain slowing compared to control. Conclusion:Our findings indicate that prolonged exposure to HET and HSD intakes synergistically increased renal p38 MAPK and circulatory product of oxidative cellular damage without alteration in circulatory HSP70 and NO.

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Plasma osmolality (pOsmol) and neurohumoral signals play important roles in the pathophysiology of cardiovascular diseases. Our study investigated the effect of high environmental temperature (HET) on neurohumoral responses and pOsmol in rats fed a high salt diet (HSD), with and without angiotensin II receptor blockade (ARB), using telmisartan.  Fifty-six male 8-week old Sprague-Dawley rats (95-110g) were randomly assigned into seven groups of 8 rats. These included control rats (I) fed with 0.3% NaCl diet (normal diet, ND); salt-loaded rats (II) fed with 8% NaCl (high salt) diet; ND rats (III) exposed to HET (38.5±0.5oC ) 4 hours daily per week; rats (IV) fed with 8% NaCl diet and exposed to HET daily. Others included rats (V) fed with 8% NaCl diet and treated with telmisartan (30mg/kg); ND rats (VI) exposed to HET and treated with telmisartan; rats (VI) fed with 8% NaCl diet, exposed to HET and treated with telmisartan. Plasma angiotensin II, aldosterone, vasopressin and norepinephrine (NE) concentrations were determined by ELISA technique; pOsmol from plasma K+, Na+ and Urea. HSD combined with HET in rats synergistically increased pOsmol (P<0.001) with an associated non-synergistic rise in fluid intake (P<0.001), fluid balance (P<0.001), plasma angiotensin II (P<0.01) and aldosterone (P<0.05), NE (P<0.001) and vasopressin (P<0.05) concentrations compared to control. Telmisartan did not alter pOsmol in all the treated-rats, but normalized fluid intake levels and plasma vasopressin in the rats exposed to either HSD or HEt alone. Prolonged exposure of rats to hot environment exacerbated the effect of excess dietary salt on pOsmol, with no effect on angiotensin II-mediated neurohumoral responses